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our study reveals that TRIB1 promotes CRC (show CALR Proteins) cell migration and invasion by up-regulating the expression of MMP-2 (show MMP2 Proteins) via the activation of FAK (show PTK2 Proteins)/Src (show SRC Proteins) and ERK (show EPHB2 Proteins) pathways, knockdown of TRIB1 expression in CRC (show CALR Proteins) cells abolishes these effects.
role of TRIB1 in cell cycle and survival that is mediated via the modulation of NFkappaB signaling.
the co-operativity observed between MYC (show MYC Proteins) and TRIB1 in the absence of PML (show PML Proteins)/RARA (show RARA Proteins) show that, outside of acute promyelocytic leukemia (show PML Proteins), gain of both genes may drive selection for trisomy 8.
The crucial role of TRIB1 in cisplatin-induced enrichment of CSC and drug resistance was verified by knockdown TRIB1. Interestingly, cisplatin treatment also contributed to the increasement of HDAC (show HDAC3 Proteins), the interaction of TRIB1 with HDAC (show HDAC3 Proteins), and inactivation of p53 (show TP53 Proteins).
Trib1 formed a complex with pHDAC1.
Studies indicate that tribbles homolog 1 (Drosophila) protein appear to be involved in some of the most common diseases, such as cancer, metabolic disease and hyperlipidaemia.
Studies suggest that pseudo-kinase family of tribbles (TRIB) proteins TRIB1, TRIB2 (show TRIB2 Proteins) and TRIB3 (show TRIB3 Proteins) play roles in pathogenesis of rheumatoid arthritis (RA) and osteoarthritis.
Studies indicate that the minor allele of a single nucleotide polymorphism (SNP, rs6982502) in the regulatory sequence reduces the activity of the tribbles homolog 1 (Drosophila) protein (TRIB1) promoter.
Studies suggest that pseudo-kinase family of tribbles (TRIB) proteins TRIB1, TRIB2 (show TRIB2 Proteins) and TRIB3 (show TRIB3 Proteins) were involved in the pathogenesis of inflammation.
Studies indicate that tribbles homolog 1 (Drosophila) protein (TRIB1) interacts with the master molecule of Tregs, forkhead box P3 (FOXP3 (show FOXP3 Proteins)), a transcription factor essential for Treg suppressive activity.
The Liver Clock Controls Cholesterol Homeostasis through Trib1 Protein-mediated Regulation of PCSK9 (show PCSK9 Proteins)/Low Density Lipoprotein Receptor (LDLR (show LDLR Proteins)) Axis.
Deletion of hepatic Trib1 leads to increased C/EBPalpha (show CEBPA Proteins) binding near upregulated lipogenic genes, as well as Trib1 itself.
TRIB1 and TRIB3 (show TRIB3 Proteins) are more strongly expressed than TRIB2 (show TRIB2 Proteins) in cumulus cells (CC) surrounding oocytes from preovulatory follicles than in CC of immature ones.
These data suggested that the modulation of TRIB1 expression affects hepatic lipogenesis and glycogenesis through multiple molecular interactions.
In gene knock-down experiments in macrophages using small interfering RNAs targeted to Trib1, it was observed that TNF-alpha production was increased following treatment with IFN-gamma and/or TLR2 ligands.
These results indicate that COP1 and Trib1 act as an oncoprotein complex functioning upstream of C/EBPalpha (show CEBPA Proteins), and its ligase activity is crucial for leukemogenesis.
tribbles-1 is a novel binding partner of Foxp3 (show FOXP3 Proteins) in regulatory T cells
results demonstrate that Trib1 is critical for adipose tissue maintenance and suppression of metabolic disorders by controlling the differentiation of tissue-resident M2-like macrophages
Trib1-knockout mice showed elevated levels of plasma TG and cholesterol due to increased VLDL production.
Trib1 transduced hematopoietic stem cells developed acute myeloid leukemia (show BCL11A Proteins).
a nuclear factor\; gene expression induced by m1-acetylcholine receptor
tribbles homolog 1 (Drosophila)
, G-protein-coupled receptor induced protein
, phosphoprotein C8FW
, tribbles homolog 1
, G-protein-coupled receptor-induced gene 2 protein
, G-protein-coupled receptor-induced protein 2
, phosphoprotein regulated by mitogenic pathways
, tribbles-like protein 1
, G-protein-coupled receptor induced protein GIG2